http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3044169/nPTLS and CFS have distinguishing CSF protein complements. Each condition has a number of CSF proteins that can be useful in providing candidates for future validation studies and insights on the respective mechanisms of pathogenesis. Distinguishing nPTLS and CFS permits more focused study of each condition, and can lead to novel diagnostics and therapeutic interventions.
I know it is a bit hard to find out some of the information here as it is a bit of a summary. They are looking at proteins in the Pooled cerebrospinal fluid of Neurologic Post Treatment Lyme disease (nPTLS) and Chronic Fatigue (CFS.
One interesting thing is that Table S5. (Pathway analysis for proteins identified only in nPTLS proteome.)

indicates that the melatonin pathway is affected in Lyme people , and not in the CFS group

I am wondering if those people with sleep disorders that can be addressed with melantonin reflect that they have lyme disease??
Also a lot of these are invoved in immunity for both Lyme and CFS, for example the Complement System and Coagulation System

Abstract
Time is a dimension tightly associated with the biology of living species. There are cycles of varied lengths in biological activities, from very short (ultradian) rhythms to rhythms with a period of approximately one day (circadian) and rhythms with longer cycles, of a week, a month, a season, or even longer. These rhythms are generated by endogenous biological clocks, i.e. time-keeping structures, rather than being passive reactions to external fluctuations. In mammals, the suprachiasmatic nucleus (SCN) is the major pacemaker. The pineal gland, which secretes melatonin, is the major pacemaker in other phyla. There also exist biological clocks generating circadian rhythms in peripheral tissues, for example the liver. A series of clock genes generates the rhythm through positive and negative feedback effect of proteins on their own synthesis, and this system oscillates with a circadian period. External factors serve as indicators of the astronomical (solar) time and are called zeitgebers, literally time-givers. Light is the major zeitgeber, which resets daily the SCN circadian clock. In the absence of zeitgebers, the circadian rhythm is said to be free running; it has a period that differs from 24 hours. The SCN, together with peripheral clocks, enables a time-related homeostasis, which can become disorganized in its regulation by external factors (light, social activities, food intake), in the coordination and relative phase position of rhythms, or in other ways. Disturbances of rhythms are found in everyday life (jet lag, shift work), in sleep disorders, and in several psychiatric disorders including affective disorders. As almost all physiological and behavioural functions in humans occur on a rhythmic basis, the possibility that advances, delays or desynchronization of circadian rhythms might participate in neurological and psychiatric disorders has been a theme of research. In affective disorders, a decreased circadian amplitude of several rhythms as well as a phase advance or delay have been described, leading to hypotheses about changes in biological clocks themselves or in their sensitivity to environmental factors, such as light or social cues. Molecular genetics studies have suggested the involvement of circadian clock genes, but no tight association has yet been found. Agomelatine is an antidepressant, agonist at melatonergic MT(1), MT(2) receptors and antagonist at 5-HT(2C) receptors, and is able to phase advance circadian rhythms in humans. The fact that non-pharmacological (light therapy, sleep deprivation, rhythm therapy) and pharmacological (lithium, antidepressants, agomelatine) therapies of affective disorders influence circadian rhythms indicates that biological clocks play a role in the pathophysiology of these disorders.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3044169/nPTLS and CFS have distinguishing CSF protein complements. Each condition has a number of CSF proteins that can be useful in providing candidates for future validation studies and insights on the respective mechanisms of pathogenesis. Distinguishing nPTLS and CFS permits more focused study of each condition, and can lead to novel diagnostics and therapeutic interventions.

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Certainly interesting but perhaps of concern is that although Fukada et al is referenced, there appears no clear statement about diagnostic selection, the tests having been carried out on 'banked' samples. Given the authors' use CF as interchangeable with CFS, reservations about what this means for CFS are probably warranted. Of course that doesn't change the the significance of the findings in themselves.
Misread as per post below. Fukada was used for case definition.

Given the authors' use CF as interchangeable with CFS, reservations about what this means for CFS are probably warranted.

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"CF" was never used, and "Chronic Fatigue (CFS)" was used once. After that it was called "CFS" or "Chronic Fatigue Syndrome". So in does indeed seem that they intended to say "Chronic Fatigue Syndrome", and that Fukuda CFS is what they were studying and what the results apply to.

"CF" was never used, and "Chronic Fatigue (CFS)" was used once. After that it was called "CFS" or "Chronic Fatigue Syndrome". So in does indeed seem that they intended to say "Chronic Fatigue Syndrome", and that Fukuda CFS is what they were studying and what the results apply to.

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You are right - I missed this:CFS Subjects Both pooled and individuals CSF samples were analyzed. Equal aliquots from individual CSF samples were pooled to provide sufficient volume for extensive fractionation and two-dimensional LC coupled to tandem MS (2D-LC-MS/MS) analysis with immunoaffinity depletion from 30 women and 13 men (n=43) who fulfilled the 1994 case definition for CFS [1].

AFCFS and Tania
i am wondering if this means you have Lyme disease, just a thought

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Currently trying to rule that in or out; I think the melatonin may have a small indicative role, but will not likely be the de-facto standard. I think it is likely a concomitant finding. Too many other things where others respond to melatonin, like jet lag.

REVIEWER'S CONCLUSIONS:
Melatonin is remarkably effective in preventing or reducing jet-lag, and occasional short-term use appears to be safe. It should be recommended to adult travellers flying across five or more time zones, particularly in an easterly direction, and especially if they have experienced jet-lag on previous journeys. Travellers crossing 2-4 time zones can also use it if need be. The pharmacology and toxicology of melatonin needs systematic study, and routine pharmaceutical quality control of melatonin products must be established. The effects of melatonin in people with epilepsy, and a possible interaction with warfarin, need investigation.